Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/198722
Type: Artigo de periódico
Title: Mechanism Of Trypanosoma Cruzi Death Induced By Cratylia Mollis Seed Lectin.
Author: Fernandes, M P
Inada, N M
Chiaratti, M R
Araújo, F F B
Meirelles, F V
Correia, M T S
Coelho, L C B B
Alves, M J M
Gadelha, F R
Vercesi, A E
Abstract: Incubation of T. cruzi epimastigotes with the lectin Cramoll 1,4 in Ca(2+) containing medium led to agglutination and inhibition of cell proliferation. The lectin (50 microg/ml) induced plasma membrane permeabilization followed by Ca(2+) influx and mitochondrial Ca(2+) accumulation, a result that resembles the classical effect of digitonin. Cramoll 1,4 stimulated (five-fold) mitochondrial reactive oxygen species (ROS) production, significantly decreased the electrical mitochondrial membrane potential (Delta Psi(m)) and impaired ADP phosphorylation. The rate of uncoupled respiration in epimastigotes was not affected by Cramoll 1,4 plus Ca(2+) treatment, but oligomycin-induced resting respiration was 65% higher in treated cells than in controls. Experiments using T. cruzi mitochondrial fractions showed that, in contrast to digitonin, the lectin significantly decreased Delta Psi(m) by a mechanism sensitive to EGTA. In agreement with the results showing plasma membrane permeabilization and impairment of oxidative phosphorylation by the lectin, fluorescence microscopy experiments using propidium iodide revealed that Cramoll 1,4 induced epimastigotes death by necrosis.
Subject: Animals
Calcium Signaling
Cell Membrane Permeability
Cell Proliferation
Cell Survival
Digitonin
Fabaceae
Glycoconjugates
Humans
Keratinocytes
Membrane Potential, Mitochondrial
Necrosis
Oxidative Phosphorylation
Plant Lectins
Reactive Oxygen Species
Trypanosoma Cruzi
Rights: fechado
Identifier DOI: 10.1007/s10863-010-9268-9
Address: http://www.ncbi.nlm.nih.gov/pubmed/20155390
Date Issue: 2010
Appears in Collections:Unicamp - Artigos e Outros Documentos

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